Cardiopulmonary bypass (“CPB”) is most frequently used to divert blood away from the heart and lungs during open-heart surgery or major repair of the ascending aorta. In its basic form, the bypass circuit typically includes a cannula inserted into the right atrium or one of the major veins leading to die heart, connected to tubing to transport, the patient's deoxygenated venous blood to a reservoir, the blood then being passed through a centrifugal pump to an oxygenator and heat exchanger; and tubing to carry oxygenated blood to an arterial filter and air bubble trap, the blood then being returned to the patient through a cannula in the wall of the ascending aorta or other major artery. During surgery, the heart can be paralyzed by infusing into the heart a cardioplegia solution containing a high concentration of potassium, both to allow the surgeon to control the operative field and to reduce energy and oxygen consumption by the heart muscle. Infusion of the cardioplegia solution is commonly achieved through a separate pump-driven branch circuit (“cardioplegia circuit”) of the CPB circuit, carrying chilled, oxygenated blood coming from the oxygenator/heat exchanger through tubing to a cannula inserted into the heart. An infusion pump allows for the introduction of a high concentration/low volume cardioplegia solution at a precise rate into the blood of the cardioplegia circuit. Optionally, there may also be a cardiotomy circuit comprising a suction cannula attached to a pump for aspirating shed blood in the chest cavity, the blood then being passed through a filter and into the venous reservoir, and ultimately recirculated to the patient.
The CPB circuit must be purged of air and primed with a saline solution prior to commencing bypass, which causes a substantial volume of extra fluid to be delivered to the patient. It is generally believed that the amount of volume occupying the various tubings, pumps, reservoirs and filters in a CPB circuit should be minimized in order to reduce some of the complications associated with CPB. Some of these complications include anemia and edema, as well as inflammatory responses caused by the exposure of blood to plastic components, all of which can lead to pulmonary, renal and cerebral dysfunction. These complications can be exacerbated by the damage caused to the cellular elements of the blood (such as red blood cells) by the pumps used in a typical CPB circuit. The typical CPB circuit usually includes a centrifugal pump or roller pump for the high flow-rate main circuit, and peristaltic or roller pumps for branch circuits and medication infusion lines. Any of these types of pumps can create high shear forces on the cellular elements of the blood, leading to hemolysis and platelet activation, which can have several detrimental effects on the patient. Furthermore, microemboli of air, fat, platelet aggregates, thrombi, atheromatous plaque fragments and other debris can enter the patient's circulatory system, also leading to ischemic and inflammatory events in various organs.
Efforts have been directed to reducing the size of the priming volume of CPB circuits, an example of which is described in U.S. Pat. No. 6,852,280. Shortening interconnections between devices, reducing the diameter of tubing, and minimizing the volume of the venous reservoir can lead to significant reductions in the priming volume, for example, from approximately 1700 cc's to less than 600 cc's. If the priming volume can be made sufficiently small, it may be possible to prime the CPB circuit with the patient's own blood, reducing the amount of excess fluid ultimately delivered to the patient, and thus also reducing the amount of blood transfusions needed to maintain an acceptable hematocrit. In some cases, it is possible to reduce the priming volume further by eliminating arterial-line filters and in-line blood cardioplegia. Also, using vacuum-assisted venous drainage allows for the use of smaller diameter cannulas and tubing while maintaining adequate flow rates. In other cases, it may be possible to reduce priming volume by consolidating components (such as filters, reservoirs, pumps) into single elements that require less interconnecting tubing.
However, reducing the priming volume alone does not necessarily ameliorate other major problems associated with CPB, including, for example, hemolysis and the propagation of microemboli. The incidence of stroke after cardiac surgical procedures can range from 3-9%, the highest incidence being associated with hypothermic circulatory arrest and CPB. The incidence of post-operative encephalopathy can range from 8-32%. Since the advent of newer cerebral imaging techniques that can detect brain lesions due to microemboli, many clinicians have concluded that microembolization is probably a significant contributing factor to post-CPB encephalopathy. As many as 45% of post-operative patients may exhibit brain lesions due to microemboli, despite having no signs of impaired cerebral function. (See G. McKhann et al., Stroke and Encephalopathy After Cardiac Surgery—An Update, Stroke 2006; 37:562-71). As many as 25 percent of infants undergoing CPB and deep hypothermic circulatory arrest show post-operative evidence of at least transient neurologic injury. Although the mechanisms that lead to post-operative neurological impairment are thought to be multifactorial, microembolization is considered to be significant factor.
The risk of microembolization may be increased if arterial-line filters are eliminated; and there may be increased risk of air embolization with the use of vacuum-assisted venous drainage, or if venous reservoirs are bypassed. Thus, there is a trade-off between the desire to minimize the priming volume and the need to minimize microembolization (See B. Alsoufi et al, Hypothermia, Circulatory Arrest and Cardiopulmonary Bypass, available at www.emedicine.com/ped/TOPIC2813.HTM (article last updated Aug. 1, 2006)).
Concerns have also been raised about the potential detrimental effects of continuous flow vs. pulsatile flow in both CPB and in other forms of assisted circulation. Absence of pulsatile blood flow could lead to a loss of baroreceptor-mediated control of blood circulation in the patient, and result in a decrease in regional blood flow and oxygen delivery. Non-pulsatile perfusion during CPB may have an adverse effect on renal function (See F. Onorati et al., Am. J. Kidney Dis. 2007 August; 50(2):229-38). Adding pulsatile flow from an intra-aortic balloon pump during CPB may help to preserve lung function in patients with chronic obstructive pulmonary disease (See F. Onorati, et al, Ann. Thorac. Surg. 2006 July; 82(1):35-43). Use of pulsatile flow during CPB in children undergoing heart surgery for repair of congenital heart defects may improve cardiac, renal and pulmonary functions in the early post-CPB period (See T. Alkan et al, ASAIO J. 2007 November-December; 53(6):651-4). There have been various attempts to introduce pulsatile blood flow during CPB. For example, U.S. Pat. No. 6,620,121 describes the use of a pulse wave generator for CPB, consisting of a compression assembly acting on an in-line collapsible chamber placed downstream from a roller pump and membrane oxygenator. However, most of these attempts require the addition of devices to the CPB circuit, increasing their complexity, the priming volume and the opportunity for additional shear stress to be applied to the cellular elements of the blood.
There remains a need for an improved CPB apparatus and method, having a reduced priming volume, simplified extracorporeal circuit, and having pump and valve control systems that simplify and increase the reliability and precision of the operation of CPB apparatus. Moreover, there continues to be a need to incorporate pumps that have the ability to meet the flow requirements of CPB and yet minimize trauma to the blood. Furthermore, it would be advantageous to have CPB apparatus with the flexibility to introduce pulsatile flow if desired, and that can employ modular elements to reduce costs and increase the flexibility of using the equipment in a variety of settings.